title: A technological advance comparing epithelial lining fluid from different regions of the lung in smokers.
abstract: Cigarette smoking causes inflammatory responses in the airways. However, not all smokers exhibit the development of airflow limitation. This study was designed to determine the implications of small airways inflammation in the development of airflow limitation in smokers by our newly explored method. Twenty-eight smokers (15 smokers without airflow limitation and 13 with airflow limitation) were included in this study. Levels of interleukin-8 (IL-8) and 8-isoprostane were measured in epithelial lining fluid (ELF) from central and peripheral airways separately collected using a bronchoscopic microsampling technique. 8-isoprostane levels in ELF from central or peripheral airways did not significantly differ between the two groups. However, these levels were markedly higher in peripheral than in central airways. Similarly, IL-8 levels in ELF from central airways did not significantly differ between the two groups. In smokers without airflow limitation, IL-8 levels were not higher in peripheral than in central airways. In contrast, in smokers with airflow limitation, IL-8 levels were significantly higher in peripheral airways. Moreover, in smokers with airflow limitation, 8-isoprostane levels in central or peripheral airways were not significantly correlated with FEV(1). However, IL-8 levels in peripheral airways were inversely correlated with FEV(1), though those levels in central airways were not. Thus our technique provides a novel method for ELF sampling from central or peripheral airways separately, and the preliminary evidence that support differences in oxidative stress and neutrophil chemotactic stimulus in these two locations.
authors.affiliation: Department of Respiratory Medicine, Graduate School of Medicine, Osaka City University, 1-4-3 Asahi-machi, Abenoku, Osaka 545-8585, Japan.
authors.forename: Toyoki
authors.initials: T
authors.lastname: Kodama
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kanazawa
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Tochino
authors.forename: Shigenori
authors.initials: S
authors.lastname: Kyoh
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Asai
authors.forename: Kazuto
authors.initials: K
authors.lastname: Hirata
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000032:analysis; D001980:Bronchi; D055745:Bronchioles; D001988:Bronchiolitis / Q000276:immunology / Q000503:physiopathology; D001991:Bronchitis / Q000276:immunology / Q000503:physiopathology*; D001999:Bronchoscopy / Q000379:methods; D015237:Dinoprost / Q000031:analogs & derivatives / Q000032:analysis / Q000378:metabolism; D045604:Extracellular Fluid / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D020545:Respiratory Mucosa / Q000276:immunology / Q000378:metabolism*; D012907:Smoking / Q000009:adverse effects*; D018709:Statistics, Nonparametric
chemical_list: D015415:Biomarkers; D016209:Interleukin-8; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost